Chronic insomnia linked to faster cognitive decline and brain aging

A new study reports that individuals with chronic insomnia may face a more rapid decline in memory and thinking abilities as they age. Published in Neurology, the medical journal of the American Academy of Neurology, the research also found that these cognitive changes correspond with physical alterations in the brain visible on imaging scans. The findings suggest that long-term sleep difficulties are associated with brain aging, although the study does not establish that insomnia directly causes this process.

Researchers have long suspected a link between poor sleep and cognitive problems, but many previous studies had limitations. These earlier investigations often did not account for other co-occurring health issues that could influence the results, such as obstructive sleep apnea or the use of sleep medications.

The lead author of the new study, Diego Z. Carvalho of the Mayo Clinic, and his colleagues wanted to conduct a more comprehensive analysis. Their goal was to clarify the relationship between insomnia and cognitive decline while also exploring the specific underlying brain pathologies, such as changes related to Alzheimer’s disease or to the brain’s blood vessels.

The investigation drew upon data from the Mayo Clinic Study of Aging, a long-term project that follows residents of Olmsted County, Minnesota. The researchers included 2,750 participants aged 50 and older who did not have major neurological or psychiatric disorders at the outset. To identify individuals with chronic insomnia, the team reviewed electronic medical records for documented insomnia diagnoses that occurred at least 30 days apart. This method resulted in a group of 443 people with chronic insomnia and a comparison group of 2,307 people without.

All participants underwent regular and thorough cognitive evaluations, which assessed memory, language, executive function, and visual spatial skills. These scores were combined to create a global measure of cognitive health, allowing the researchers to track changes over time. The team also monitored participants for the new onset of mild cognitive impairment or dementia.

A subset of the participants received brain scans. Magnetic resonance imaging was used to measure the volume of white matter hyperintensities, which are small areas of damage often linked to problems with the brain’s blood supply. Positron emission tomography scans were used to measure the amount of amyloid plaques, which are protein deposits strongly associated with Alzheimer’s disease.

The study found a clear association between chronic insomnia and accelerated cognitive aging. Individuals with chronic insomnia experienced a faster decline in their global cognitive scores over the study period. Their risk of developing mild cognitive impairment or dementia was 40% higher than that of people without insomnia. The researchers calculated that this increased risk was equivalent to the effect of being 3.5 years older.

A more detailed analysis revealed that the combination of insomnia and a self-reported reduction in sleep duration was particularly significant. People who had both chronic insomnia and reported sleeping less than usual had lower cognitive scores at the beginning of the study compared to other participants. This suggests that the negative effects may have been present even before the formal tracking began.

The brain imaging results provided physical evidence that may help explain these cognitive findings. The group with both insomnia and reduced sleep had a greater volume of white matter hyperintensities at the start of the study. These brain lesions suggest a link between this specific sleep profile and cerebrovascular disease, which affects the small blood vessels in the brain. In contrast, participants with insomnia who reported sleeping more than usual had a lower volume of these white matter changes, indicating a potentially different relationship with brain health.

The scans also showed a connection to Alzheimer’s disease pathology. Participants with insomnia and reduced sleep had higher levels of amyloid plaques in their brains at baseline. The magnitude of this effect was comparable to carrying the APOE e4 gene, a well-known genetic risk factor for Alzheimer’s disease. This finding suggests that poor sleep may be connected to the accumulation of proteins that are a hallmark of the neurodegenerative disorder.

“Insomnia doesn’t just affect how you feel the next day—it may also impact your brain health over time,” said Carvalho. “We saw faster decline in thinking skills and changes in the brain that suggest chronic insomnia could be an early warning sign or even a contributor to future cognitive problems.”

The research team also examined the potential role of hypnotic medications, often prescribed for sleep. In this study, the use of these medications was not associated with faster cognitive decline or with the brain changes observed on scans. These findings may offer some reassurance to individuals who rely on such treatments, though the researchers note that more detailed investigation is needed.

“Our results suggest that insomnia may affect the brain in different ways, involving not only amyloid plaques, but also small vessels supplying blood to the brain,” Carvalho said. “This reinforces the importance of treating chronic insomnia—not just to improve sleep quality but potentially to protect brain health as we age. Our results also add to a growing body of evidence that sleep isn’t just about rest—it’s also about brain resilience.”

The study has several limitations that the authors acknowledge. The diagnosis of insomnia was based on medical records rather than standardized interviews for every participant. Sleep duration was self-reported and not measured objectively with sleep-monitoring devices. The data on hypnotic medication use did not include details about dosage, frequency, or duration of treatment. Finally, the study population was predominantly white, which means the findings may not apply to more diverse populations.

Future research should aim to confirm these results using objective sleep measures and more diverse cohorts. It will also be important to investigate whether effectively treating insomnia, through methods like cognitive behavioral therapy or specific medications, can slow or prevent cognitive decline and the associated brain changes. Such studies could help determine if improving sleep is a viable strategy for promoting long-term brain health.

The study, “Associations of Chronic Insomnia, Longitudinal Cognitive Outcomes, Amyloid-PET, and White Matter Changes in Cognitively Normal Older Adults,” was authored by Diego Z. Carvalho, Bhanu Prakash Kolla, Stuart J. McCarter, Erik K. St. Louis, Mary M. Machulda, Scott A. Przybelski, Angela J. Fought, Val J. Lowe, Virend K. Somers, Bradley F. Boeve, Ronald C. Petersen, Clifford R. Jack, Jonathan Graff-Radford, Andrew William Varga, and Prashanthi Vemuri.